Rethinking the Treatment of Diabetes

The first time I presented medical research findings, I was not yet a physician. The year was about 1975. I was in my early forties and a mid-career engineer. The forum was a scientific symposium on diabetes. At the time, I felt that I had discovered the holy grail of diabetes care and was eager to share what I had learned.

By normalizing my blood sugars, I had nearly eliminated the hypoglycemic episodes that had been an almost daily occurrence for me, and slowly, with normal blood sugars, I had begun to reverse many of the complications I had accrued since my diagnosis as a type 1 in 1946.

Thanks to some fortunate circumstances, when the first three-pound blood sugar meters became available in 1969, I secured one. At the time they were a niche device, intended for emergency rooms, and only hospitals and physicians could acquire them. They were hardly envisioned as the multibillion dollar industry of today. My wife, a physician, helped me buy that first one, for the princely sum of $650.

I learned through trial and error that I could actually bring my blood sugars into a normal range and keep them there. I also learned that by controlling my diet-eliminating foods that caused considerable elevations in blood sugar, particularly simple carbohydrates such as starches and sugars-I could significantly reduce my dosage of insulin and thus reduce its unpredictability. By 1973, I had seen such important changes in my own health and the reversal of my complications that I attempted to persuade physicians specializing in diabetes to give my method (which also included basal/bolus insulin dosing) a try.

By the time I gave my talk, I had persuaded two physicians doing diabetes research to study the effects of blood sugar normalization on diabetic complications. Both studies were really the first of their kind. And both showed reversal of early diabetic sequellaei,ii. Each also included a mental health aspect (because “the experts” were convinced that the studies were going to drive the participants crazy). In both studies, depression scores plummeted from severely depressed to normaliii,iv.

At that symposium, contrary to my naïve image of the world beating a path to my door because of my better mousetrap, my talk was met with indifference by the physicians there. (The few patients present, however, surrounded me afterward and bombarded me with questions.) Self-monitoring to help control blood sugars was a curiosity, nothing more.

I struggled for opportunities to present my discoveries, but for the most part, there were no takers in the U.S. and a very few overseas. I tried to get medical journals to publish my findings, but the use of an “electrical device” to guide the treatment of diabetes was repeatedly ridiculedv. After a while, I realized that the only way I would get published would be with an MD after my name.

In 1982, at age 48, I received my MD. A year later, I began my private practice. Because I was a type 1 diabetic and had developed my protocols on that model, I thought I was mainly going to be treating type 1 diabetics. It turned out, however, that there were many more type 2s who needed my help.

At that time, there were about 6 million known diabetics in the U.S. I then had every reason to assume that because my first bookvi was already in print, my guidelines for treatment and prevention would be widely adopted. I may have been overly optimistic, but there was good reason for such hope. Evidence had accumulated that normal blood sugars not only reversed complications, but also prevented insulin-producing beta cells from burning out.

The current excuse that normal blood sugars cause severe hypoglycemia is borne of the common practice of treating diabetes with large amounts of carbohydrate covered by industrial doses of insulin or sulfonylureasvii,viii. The justification for this practice is the now disproved mythix that low carbohydrate/high protein diets cause dyslipidemia and nephropathy.

At about the time I started my practice, Gerald Reaven, author of Syndrome X, used the Biostator GCIIS, an “artificial pancreas,” to normalize the blood sugar of 32 patients for two weeks. The cumbersome and expensive device constantly measured blood sugar and clamped it at 90 mg/dl. One outcome was that high A1c levels dropped dramatically. The study then followed the patients, half of them male, half female, and also found that it took two years of ordinary living [and likely inappropriate diet] for theirA1c’s to return to pre-study levels. To me this implied the most important finding-that beta cell burnout dysfunction could be halted or reversed by a combination of exogenous insulin and normal blood sugars. By giving overworked beta cells a rest, they could improve or regain function. A similar study by a Taiwanese group recently came to the same conclusionx.

It is usually easy to treat diabetics who make insulin, and the more insulin they make, the easier it is to treat them. The bulk of the type 2 patients I see make too little insulin to overcome their insulin resistance, so I may start them on at least a small amount of injected insulin. The problem with injected insulin is that large doses cannot be absorbed predictably. So the more insulin a patient must inject, the higher the likelihood of unpredictable blood sugars. This is typically the case when physicians prescribe high carbohydrate diets and then cover the carbohydrate with large doses of insulinxi.

Despite my own story and Reaven’s important findings, the techniques I developed have been only superficially adopted, even all these years later. There are no “expert” guidelines for beta cell preservation, and sulfonylurea drugs, which hasten beta cell deterioration, are still widely prescribed. The same is true for high carbohydrate diets covered by industrial doses of insulin.

We now have an epidemic of diabetes, with some 20 million or more diabetics in the U.S., and the increase shows no signs of slowing. The epidemic is a multi-hundred billion dollar drag on our already overburdened healthcare system and fragile economy

Medical students, a recent study found, avoid specializing in diabetes care for a variety of reasons, mostly related to the hopelessness of current treatmentxii. That’s probably because standard treatment these days doesn’t work.

I read decades ago that blood sugar normalization might reverse diabetic complications for animals, but “the experts” claimed it would never be of value to humans. The new generation of experts still denigrates the practice. “People just won’t be bothered,” they say. If medical students feel hopeless about diabetes care, imagine how the diabetics themselves must feel.

With current guidelines, it’s small wonder that people – diabetics and those who treat them – feel hopeless.

The current “wisdom” is that pre-prandial blood sugars should be as high as 130 mg/dl and postprandial blood sugars as high as 180 mg/dl -more than double normal. The only “complication” that those high blood sugars will prevent is hypoglycemia. Patients are likewise instructed that an A1c is normal if less than 6.0 percentxiii (or the equivalent of an average blood sugar of 140mg/dlxiv) when studies of non-diabetics show that 6 percent applies only to people over the age of 70xv.

As dangerous as a severe hypoglycemic event can be, it’s relatively easy to monitor for and correct. Complications that are vastly more serious and debilitating are inevitable with chronically elevated blood sugars. (I have found that my patients with normalized blood sugars rarely have severe hypoglycemic episodes, and far less frequently than I’ve seen in conventionally treated diabeticsvii,viii.) To those who guide the guidelines, the significant difference between a severe hypoglycemic episode and a stroke or heart attack is that while the latter are seen as natural consequences of diabetes, a physician can be sued if a patient dies from a hypoglycemic event. Thus current guidelines of care have been devised to protect the physician rather than the patient.

My position is this: people don’t die from diabetes. They die from the complications of diabetes. I and others have shown that blood sugar normalization can prevent or reverse the complications of diabetes.

My blood sugars have been virtually normal for more than 40 years. Most of my patients’ blood sugars and lipid profiles have dramatically improved and are usually normal. I have many patients on whom other specialists have given up who have come to me and learned how to easily normalize their blood sugars.

If the medical community is going to make any headway against the epidemic of diabetes, then the experts are going to have to change their attitude toward blood sugar normalization. We must condemn the ready availability of cheap, simple carbohydrates and the official praise for their role in a “healthy diet,” which is becoming more commonly recognized as the leading cause of the epidemic of diabetesxi.

I’ve learned from many of my patients that carbohydrate craving is almost like an addiction-once you get off “the stuff,” you are less likely to crave it. It’s also been shown repeatedly that a diet consisting mainly of protein plus minimal amounts of slow-acting carbohydrate or whole plant vegetables, leafy greens, and similar foods helps people achieve a sense of satiety that far outlasts that of simple sugars such as those found in starches (including whole grain breads)xi.

It’s been a long time since that day when I first presented my findings, and my naïveté has been transformed to sadness. While there are many areas of diabetes care that could be drastically improved, here are a handful that can have a profound impact and are not difficult to implement.

Preventing unnecessary amputations is one. Over the past 26 years, in my capacity as director of the peripheral vascular disease clinic of a large metropolitan hospital and as a Fellow of the American College of Certified Wound Specialists, I’ve seen many diabetics post-amputation, and many more with ulcers of the feet.

Virtually all of the amputations have resulted from compliance with the current guideline that “a callus can be debrided with a scalpel by a foot care specialist or other health personnel.”xvi That’s just wrong. A callus is a symptom of pressure or shear forces and is protective rather than harmful. If it is aesthetically distasteful, the proper treatment-which requires little training-is the elimination of the pressure or shear forces that caused the callus. This is called “offloading” and is achieved by shoe modification or the use of orthotic shoe inserts. I cannot accept amputation as the solution for a callus.

Preservation of beta cell function is another. As noted above, the treatment of diabetes is much easier when a patient still has functioning beta cells. Every effort should be made to preserve beta cell function, if only to facilitate an eventual cure if the killer T cells responsible for beta cell destruction are ever isolated.

I have repeatedly seen children in the “honeymoon” stage of type 1 diabetes whose parents have been told by their specialist that their children should not inject insulin until their beta cells have burned out. I likewise see type 2s who have received similar instructions. Maybe this is done to delay fears of “painful” injections. The fact is, injections need not be painful if a more benign injection technique is followedxvii. But the consequences of not having them when they’re indicated certainly can lead to substantial pain over the long term. That kind of “care” will make patients much harder to treat in the future and likely lead to the usual consequences of chronic hyperglycemia. I’d rather see them live until there’s a cure-which just might require some healthy beta cellsx.

To put it in the simplest possible terms, the complications of diabetes are caused by long-term hyperglycemia. Hyperglycemia is caused by the failure of the body to adequately maintain blood sugar at normal levels. Intervention through dietary restrictions of simple and total carbohydrates, regular blood sugar monitoring, medication, and, when appropriate, basal/bolus dosing of insulin can normalize blood sugars. Overeating and excessive body weight can now usually be controlled by the use of self-injected synthetic Amylin and GLP-1xviii, a far more benign approach than the gastric banding/bypass surgery currently recommended. By blood sugar normalization, complications can be prevented or reversed and many deaths can be prevented. So common sense would dictate that if we, as a medical community, are considering the well-being of the patient, we should start at blood sugar normalization.

Better treatment for diabetics is neither difficult nor risky, as some professionals advocate. Until we have a cure, normalizing blood sugars is the best solution we have, because that’s exactly what a cure will do. Why wait?

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